Circulating factors as markers and mediators of endothelial cell dysfunction in preeclampsia

During the past decade It new hypothesis has been formulated that explains many of the disparate findings associated with the pregnancy syndrome preec lampsia. With an increased awareness of the physiological significance of v ascular endothelial cell function, the seemingly unrelated signs of hyperte nsion, proteinuria, edema, and hypercoagulability have converged to provide clinical evidence of a unifying pathophysiological mechanism: systemic, ma ternal endothelial cell dysfunction. Investigators have attempted to test t his hypothesis through two approaches. The first approach involves the iden tification of in vivo markers of vascular endothelial cell injury in women with clinically evident preeclampsia. The second approach focuses on the ab ility of circulating factors derived from the serum or plasma of patients a fflicted with preeclampsia to perturb endothelial cell function in vitro. I n this review we summarize the increasingly compelling evidence that matern al vascular endothelial cells are a critical target for toxic humoral activ ities that precipitate the multifaceted preeclampsia syndrome.